Vascular endothelial growth factor (VEGF)-driven actin-based motility is mediated by VEGFR2 and requires concerted activation of stress-activated protein kinase 2 (SAPK2/p38) and geldanamycin-sensitive phosphorylation of focal adhesion kinase (Q28646403)

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English	Vascular endothelial growth factor (VEGF)-driven actin-based motility is mediated by VEGFR2 and requires concerted activation of stress-activated protein kinase 2 (SAPK2/p38) and geldanamycin-sensitive phosphorylation of focal adhesion kinase	scientific journal article

Statements

scholarly article

1 reference

3 February 2017

Vascular endothelial growth factor (VEGF)-driven actin-based motility is mediated by VEGFR2 and requires concerted activation of stress-activated protein kinase 2 (SAPK2/p38) and geldanamycin-sensitive phosphorylation of focal adhesion kinase (English)

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3 February 2017

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phosphorylation

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author name string

S. Rousseau

1

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3 February 2017

F. Houle

2

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3 February 2017

H. Kotanides

3

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3 February 2017

L. Witte

4

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3 February 2017

J. Waltenberger

5

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3 February 2017

J. Landry

6

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3 February 2017

J. Huot

7

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3 February 2017

language of work or name

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publication date

7 April 2000

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3 February 2017

Journal of Biological Chemistry

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3 February 2017

275

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3 February 2017

10661–10672

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3 February 2017

14

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3 February 2017

Vascular endothelial growth factor, a potent and selective angiogenic agent

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Indirect angiogenic cytokines upregulate VEGF and bFGF gene expression in vascular smooth muscle cells, whereas hypoxia upregulates VEGF expression only

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Hypoxia induces vascular endothelial growth factor in cultured human endothelial cells

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Endothelial receptor tyrosine kinases involved in angiogenesis.

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